Standards of Care (How I treat) INTERVERTEBRAL DISC DISEASE

Standards of Care (How I treat) INTERVERTEBRAL DISC DISEASE Richard A. LeCouteur, BVSc, PhD, Diplomate ACVIM (Neurology), Diplomate ECVN University of California Davis CA 95616 USA ralecouteur@ucdaviss.edu 76 Type I Disk Extrusion The appropriate treatment for animals with type I disk extrusion depends on an individual animal s neurological status. Medical treatment directed at decreasing spinal cord edema by means of corticosteroids is indicated only in those animals with an acute onset of neurological deficits, that are examined within eight hours of the injury. The recommended agents and dosages are as described for spinal cord trauma. The use of corticosteroids in dogs with type I disk extrusion has been associated with pancreatitis, gastrointestinal bleeding, or colonic perforations. Nonsurgical (medical or conservative) treatment is recommended for animals with apparent pain only or animals that have mild neurologic deficits but are ambulatory and have not had previous clinical signs associated with disk disease. These animals should be strictly confined to a small area such as a hospital cage or a quiet place away from other pets for at least 2 weeks, and walked (on a leash or harness) only to urinate and defecate. The objective of confinement is to allow fissures in the anulus fibrosus to heal, thus preventing further extrusion of disk material, and allowing resolution of the inflammatory reaction caused by small amounts of extruded disk material. Use of analgesics, muscle relaxants, or nonsteroidal anti-inflammatory agents, is not recommended in most cases as it is believed that their use encourages animals to exercise and risk further disk extrusion. Very cautious use of analgesics or non-steroidal anti-inflammatory agents occasionally may be indicated. However, strict confinement followed by a period of restricted exercise is imperative. Owners should also be warned that an animal s neurological status may deteriorate owing to extrusion of further disk material despite this treatment and to observe the animal very carefully. If the neurological status worsens, an animal s treatment should be reevaluated immediately. Owners should also be warned that a recurrence of clinical signs is common due to further disk extrusion at the same or a different site, and subsequent episodes may be more severe, especially in the thoracolumbar spine. Animals with severe cervical pain frequently do not respond to cage rest. These dogs often have large amounts of disk material within the spinal canal, and dogs that do not show improvement after 7 to 10 days of confinement should be evaluated further by means of radiographs and myelography, and ventral cervical decompression should be considered. Surgical disk fenestration has been recommended as a prophylactic measure to prevent further extrusion of disk material into the spinal canal. Fenestration of the disks most likely to herniate (C2-3 through C6-7 in the cervical spine and T11-12 through L3-4 in the thoracolumbar spine) is recommended in animals that have had one or more episodes of apparent neck or back pain and have evidence of intervertebral disk disease on radiographs. Various surgical techniques have been described. Fenestration of disks does not remove disk material from the spinal canal and therefore is not recommended as the sole surgical procedure in dogs that have evidence of disk material within the spinal canal and spinal cord compression on radiographs and myelography. The role of disk fenestration in the management of intervertebral disk disease is controversial. Disk fenestration in the thoracolumbar region is not easily done, and complications such as scoliosis, pneumothorax, and hemorrhage may occur. Disk fenestration in the cervical region is achieved more easily and rarely is associated with such complications. Fenestration does not prevent recurrence of disk extrusion in all animals. The effectiveness of fenestration depends largely on the amount of nucleus pulposus removed. Completion of disk fenestration is recommended at the time of spinal cord decompression. Animals with neurological deficits such as paresis or paralysis with deep pain perception

A intact, animals with recurrent bouts of apparent back or neck pain, or animals with apparent back or neck pain (or mild neurological deficits) that are unresponsive to strict confinement, should be evaluated by means of spinal radiographs, CSF analysis, and myelography. Surgical decompression of the spinal cord and removal of disk material from the spinal canal should be considered. Although many dogs with moderate or severe paresis improve neurologically if treated with cage rest, neurologic recovery is often more rapid and more complete in animals following surgical decompression of the spinal cord. In addition, the neurological status of some dogs with type I disk extrusion, especially in the thoracolumbar spine, suddenly worsens over a period of hours or days despite medical treatment. Such deterioration usually results from further disk extrusion that may result in irreversible spinal cord damage and permanent paralysis. This progression of signs always is a risk with medical treatment of animals with thoracolumbar disk disease. Progression is impossible to predict on the basis of history, clinical signs, or radiography. Owners should be made aware of treatment options and offered the opportunity of referral to an appropriate surgical facility when animals are initially presented. Surgical decompression should be done as soon as possible to prevent further spinal cord damage incurred as a result of sustained compression or further extrusion of disk material. In addition, if surgery is delayed 2 to 3 weeks, disk material hardens and becomes adherent to dura mater, and becomes difficult or impossible to remove from the spinal canal. Prognosis for neurological recovery in animals that retain deep pain perception postsurgically is fair to very good. The major factors that correlate with the degree of neurological improvement seen postsurgically are the animal s neurological status prior to surgery, the rapidity of onset of clinical signs, and the time interval between onset of clinical signs and surgical decompression. Animals that have severe neurological signs, a rapid onset of clinical signs (hours), and a long period of time before surgery generally have a prolonged recovery period and may have varying degrees of permanent neurological deficit. The incidence of recurrence of clinical signs due to disk extrusion is greater in nonsurgically than surgically treated dogs. One author found that one-third of dogs with type I disk herniation that were treated nonsurgically had a recurrence of clinical signs, and generally showed greater severity of neurological deficits at the time of recurrence. Another author reported a recurrence rate of 40 per cent in nonsurgically treated dogs. The advantages and disadvantages of various techniques for spinal cord decompression have been discussed. Surgical treatment is not without risks. Anesthesia is necessary, and surgery occasionally results in further spinal cord damage due to surgical manipulation. Nonsurgical treatment should be attempted in animals that are poor anesthesia or surgical candidates or if surgical treatment is not possible financially. In animals with clinical signs of a complete transverse myelopathy, without deep pain perception for a period of more than 24 hours, the prognosis for return of spinal cord function is poor despite medical or surgical treatment. Some of these animals may improve neurologically if given sufficient time. However, it is a matter of controversy whether surgical treatment increases the probability of improvement or not. In cases in which deep pain perception has been absent for less than 24 hours, the prognosis for return of spinal cord function is poor. However, surgical treatment may increase the likelihood of neurological improvement in this group. Regardless of whether medical or surgical treatment is instituted, animals that are paretic or paralyzed require intensive nursing care. Neurological improvement may take weeks or months and this requires owner cooperation and enthusiasm regarding care and physical therapy. Manual expression, intermittent catheterization, and /or indwelling catheterization of the bladder are often required to ensure emptying of the bladder. Weekly urinalysis, especially in animals that do not have voluntary control of micturition, is important in monitoring for urinary tract infection. It is also important to keep animals well padded, clean, and dry to prevent formation of pressure sores, and to ensure that caloric and water intake is adequate. Physical therapy does not result in neurologic improvement but helps to prevent disuse muscle atrophy associated with paraplegia or tetraplegia. Physical therapy should not be attempted in animals treated medically for at least the first 2 weeks following onset of signs, as further extrusion of disk material may occur. Type II Disk Protrusion Treatment with corticosteroids may result in neurological improvement for variable periods of time in animals with type II disk protrusion. However, corticosteroid therapy is not curative. The reason for this improvement is not clear, as intramedullary hemorrhage and edema seen in cases of acute spinal cord injury are not a feature of chronic spinal cord compression. In the thoracolumbar spine, surgical removal of protruded disk material may result in clinical improvement. However, the neurological status of some dogs is worsened permanently 77

despite careful surgical technique. The reasons for this are not known, but increased vascular permeability has been described in the spinal cord associated with release of chronic spinal cord compression and this probably plays a role in this phenomenon. Ventral decompression in the cervical spine allows removal of protruded type II disk material and neurologic improvement may occur over several months; however, some dogs, especially those with moderate to severe neurologic deficits prior to surgery, may manifest temporary or permanent worsening of clinical signs postoperatively. Standards of Care (How I Treat) DISCOSPONDYLITIS Richard A. LeCouteur, BVSc, PhD, Diplomate ACVIM (Neurology), Diplomate ECVN University of California Davis CA 95616 USA ralecouteur@ucdaviss.edu 78 Etiology and Pathogenesis Bacterial or fungal infection of the intervertebral disks and adjacent vertebral bodies (diskospondylitis), or of only the vertebral bodies (spondylitis), may result in extradural spinal cord or cauda equina compression due to granulation tissue, bony proliferation, or pathologic fracture or luxation. Less commonly, diskospondylitis may lead to diffuse or focal meningitis and myelitis. Diskospondylitis and spondylitis result from implantation of bacteria or fungi introduced by migrating plant awns (grass seeds, foxtails), hematogenous spread, extension of a paravertebral infection, a penetrating wound, or previous disk or vertebral surgery. Diskospondylitis and spondylitis occur more commonly in dogs in areas where grass awn infections are a problem. Several theories exist to explain migration of grass awns to the vertebral column. Awns may be swallowed and migrate through the bowel wall (possibly at the caudal duodenal flexure), through the mesentery to the attachment to ventral epaxial muscles, and to the vertebral column. Evidence of scarring, however, has not been found in the gut or abdomen of dogs with diskospondylitis. As dogs with diskospondylitis thought to be due to plant awn migration have lesions most commonly in the cranial lumbar spine (L2-L4) it has been suggested that awns may be inhaled and migrate through the lungs to the diaphragm, and lodge at the crural insertion on the lumbar vertebrae. Plant awns may also migrate through skin and paravertebral or abdominal muscles to the vertebral column. Grass seeds are able to travel long distances owing to the direction of the barbs. Forward progress may be aided by muscle movements. Hematogenous spread of bacteria or fungi is probably the most common cause of diskospondylitis. Sources of infection include bacterial endocarditis, sites of dental extraction., and urinary tract infections. Retrograde flow in the vertebral veins has been suggested as a possible route of infection to the vertebral column. Many dogs with diskospondylitis have concurrent urinary tract infection. Diskospondylitis due to Brucella cants infection most likely results from bacteremic spread from a genital infection. Affected intervertebral disks may have evidence of degeneration (collapsed disk space, spondylosis deformans) or trauma (traumatic disk protrusion, vertebral luxation). Prior disease or injury to the disk has been suggested as a factor in the pathogenesis of diskospondylitis. Diskospondylitis may occur with increased frequency in immunocompromized animals. Diskospondylitis and vertebral osteomyelitis also have been reported associated with Mycobacterium avium infection in basset hounds in which an inherited immunodeficiency was suggested as a predisposing factor German shepherd dogs may be predisposed to fungal diskospondylitis.

A Organisms most commonly isolated from blood, affected vertebrae, and urine of dogs with diskospondylitis are coagulase-positive Staphylococcus spp (aureus, intermedius). Other organisms isolated include Bacteroides capillosus, Brucella canis, Nocardia sp, Streptococcus canis, Corynebacterium sp, Escherichia coli, Proteus sp, Pasteurella sp, Paecilomyces sp, Aspergillus sp, and Mycobacterium sp. Coccidioides immitis may cause vertebral body osteomyelitis. Hepatozoon canis infection has been associated with periosteal bone proliferation of the vertebrae as well as other bones of the body. Spirocerca lupi infection may cause productive bony changes on the ventral aspect of thoracic vertebrae where the aorta and the esophagus run in parallel course. Clinical Findings Diskospondylitis may occur in dogs or cats of any age, however it is most commonly seen in giant and large breeds of dog. Any level of the vertebral column may be affected by diskospondylitis, and multiple lesions may be seen, in either adjacent vertebrae or nonadjacent vertebrae. Diskospondylitis occurs more commonly in thoracic and lumbar spine than in cervical spine. The lumbosacral disk space frequently is involved. Clinical findings depend on the location of the affected vertebra or vertebrae. The most common clinical signs are weight loss, anorexia, depression, fever, reluctance to run or jump, and apparent spinal pain (which may be severe). Hyperesthesia may be present only over the site of the lesion or may be poorly localized, especially with involvement of multiple sites. Diagnosis Diagnosis may be difficult, as clinical signs often are nonspecific. Diskospondylitis should always be considered in an animal with fever of unknown origin. If the lumbosacral intervertebral disk is involved, dogs often show a stilted, shortstrided pelvic limb gait and shifting pelvic limb lameness. Clinical signs commonly are present for several weeks or months before a diagnosis of diskospondylitis is made. Neurologic deficits associated with spinal cord or cauda equine compression may be present, and may reflect either a transverse or a multifocal myelopathy. Cervical lesions most commonly cause only apparent cervical pain, and lumbosacral lesions may cause neurologic deficits due to compression of nerves of the cauda equine. Rarely, animals may demonstrate clinical signs of diffuse suppurative meningitis associated with extension of infection to involve the spinal meninges. Dogs may have a history of draining tracts in the paravertebral area associated with grass seed migration. Affected animals may have a normal or elevated peripheral white blood cell count. Typical radiographic findings are destruction of the bony end-plates adjacent to an infected disk, collapse of the intervertebral disk, and varying degrees of new bone production. Early lesions may consist only of lytic areas in affected vertebral endplates. More advanced lesions show a mixture of bone lysis and extensive new bone production, with osteophytes bridging adjacent vertebrae containing a central destructive focus. Affected vertebral bodies may be shortened, and bony proliferation may result in fusion of one or more vertebrae. Infection may be difficult to distinguish from a healing fracture, unstable fracture, congenital malformation, or postoperative changes. Diskospondylitis usually can be distinguished from a neoplastic lesion, as neoplasms rarely cross intervertebral disk spaces. Diskospondylitis may be present in more than one site in the vertebral column, therefore, it is important to radiograph the entire spine in animals suspected to have diskospondylitis. Occasionally, clinical signs may occur before characteristic radiographic changes are evident. If diskospondylitis is suspected, and characteristic lesions cannot be found, a dog should be radiographed again in 2 to 4 weeks. Advanced imaging (CT or MRI) may be useful in identification of subtle vertebral lesions. Collection of CSF is indicated in animals with neurologic deficits. The CSF white blood cell count may be normal, or may be elevated, with an increase in PMN neutrophils in CSF from animals with meningitis or myelitis. Myelography is indicated in animals with neurologic deficits indicative of spinal cord compression and is mandatory in cases in which decompressive surgery is considered. Aerobic, anaerobic, and fungal cultures of blood and urine should be done prior to treatment in an attempt to isolate causative organisms. Cultures of CSF are indicated if the WBC count is elevated. Cultures of fluid from draining sinuses may also be done. Efforts should be made to diagnose B. Canis infection in all dogs with diskospondylitis. Surgical biopsy may be indicated in affected dogs in which a causative organism is not isolated from blood or urine, and/or animals that are unresponsive to treatment with broad spectrum antibiotics. Fluoroscopy-guided needle aspiration of lesions is possible in some animals. However, 79

cultures of samples collected in this way are often negative, especially if animals have been treated with antibiotics prior to completion of a biopsy. Treatment Treatment consists of long-term use of an antimicrobial that is effective against the causative organism(s) determined by results of blood and/or urine cultures. If an organism is not cultured, dogs without severe neurologic deficits may be treated empirically, assuming infection with the most common organism isolated from animals with diskospondylitis (coagulase-positive Staphylococcus sp). Antibiotics that are most effective for this purpose are cephalosporins, or beta-lactamase resistant penicillins such as oxacillin and cloxacillin. A trimethoprim/ sulfonamide combination or chloramphenicol is less effective but is less expensive, and may be effective in some cases. Clinical signs may recur if the infection is not completely eliminated prior to cessation of antibiotic therapy, and repeated cultures of blood and urine and ongoing treatment with an appropriate antibiotic may be necessary. Treatment is continued for at least 6 weeks, and vertebral radiographs are done every 4-6 weeks to monitor progression/ regression of a lesion, and to monitor for development of new lesions. Antibiotic administration may be necessary for up to 6 months before radiographic evidence of resolution of lesions is seen. A combination of minocycline or tetracycline and streptomycin is recommended for treatment of B. canis infections. Infected dogs should be neutered to eliminate risk of transmission. B. canis infections have public health significance, as people may become infected. Clinical improvement in animals with diskospondylitis (resolution of fever, improved appetite, reduction of apparent spinal pain) should be seen within 2 weeks of starting antibiotic therapy. If clinical improvement is not seen, treatment should be reevaluated. Fungal infection should be considered in animals non responsive to antibiotic therapy. Use of analgesics and restriction of exercise during the first weeks of treatment may be helpful. Surgical exploration of a lesion should be considered in animals that are unresponsive to treatment or have persistent draining tracts suggestive of grass seed migration. Objectives of surgery are curettage of lesions and harvesting of material for bacterial and fungal culture. Decompressive surgery is indicated if evidence of spinal cord compression is found on myelography and if animals show severe or progressive neurologic deficits. Surgical stabilization of the vertebrae may be necessary following decompression. Prognosis for animals with diskospondylitis depends on the ability to eliminate the causative organism(s) and on the degree of neurologic dysfunction. Animals with severe neurologic deficits and fungal infections have a guarded to poor prognosis. 80